| DBF4, not DRF1, is the crucial regulator of CDC7 kinase at replication forks. | DBF4, not DRF1, is the crucial regulator of CDC7 kinase at replication forks.
Göder A, Maric CA, Rainey MD, O'Connor A, Cazzaniga C, Shamavu D, Cadoret JC, Santocanale C., Free PMC Article | 06/13/2024 |
| The prognostic significance and potential mechanism of DBF4 zinc finger in hepatocellular carcinoma. | The prognostic significance and potential mechanism of DBF4 zinc finger in hepatocellular carcinoma.
Wu Z, Zhang L, Li X, Liu L, Kuang T, Qiu Z, Deng W, Wang W., Free PMC Article | 05/13/2024 |
| DBF4 Dependent Kinase Inhibition Suppresses Hepatocellular Carcinoma Progression and Potentiates Anti-Programmed Cell Death-1 Therapy. | DBF4 Dependent Kinase Inhibition Suppresses Hepatocellular Carcinoma Progression and Potentiates Anti-Programmed Cell Death-1 Therapy.
Zhang L, Hong J, Chen W, Zhang W, Liu X, Lu J, Tang H, Yang Z, Zhou K, Xie H, Jia C, Jiang D, Zheng S., Free PMC Article | 09/8/2023 |
| Identification and Validation of a Prognostic Model Based on Three MVI-Related Genes in Hepatocellular Carcinoma. | Identification and Validation of a Prognostic Model Based on Three MVI-Related Genes in Hepatocellular Carcinoma.
Tang Y, Xu L, Ren Y, Li Y, Yuan F, Cao M, Zhang Y, Deng M, Yao Z., Free PMC Article | 04/2/2022 |
| Molecular functions of ASK family in diseases caused by stress-induced inflammation and apoptosis. | Molecular functions of ASK family in diseases caused by stress-induced inflammation and apoptosis.
Kojima K, Ichijo H, Naguro I. | 07/31/2021 |
| High DBF4 expression is associated with oral cancer. | Cdc7-Dbf4-mediated phosphorylation of HSP90-S164 stabilizes HSP90-HCLK2-MRN complex to enhance ATR/ATM signaling that overcomes replication stress in cancer.
Cheng AN, Fan CC, Lo YK, Kuo CL, Wang HC, Lien IH, Lin SY, Chen CH, Jiang SS, Chang IS, Juan HF, Lyu PC, Lee AY., Free PMC Article | 08/10/2019 |
| CDC7-DBF4 kinase (DDK) has a primary role in the replication checkpoint to promote single-stranded DNA accumulation at stalled forks, which is required to initiate a robust checkpoint response and cell cycle arrest to maintain genome integrity. | DDK Has a Primary Role in Processing Stalled Replication Forks to Initiate Downstream Checkpoint Signaling.
Sasi NK, Coquel F, Lin YL, MacKeigan JP, Pasero P, Weinreich M., Free PMC Article | 02/2/2019 |
| Both CDC7 and DBF4 promoters bind E2F, suggesting that increased E2F activity in RB1 mutant cancers promotes increased DDK expression. Surprisingly, increased DDK expression levels are also correlated with both increased chemoresistance and genome-wide mutation frequencies. | DDK Promotes Tumor Chemoresistance and Survival via Multiple Pathways.
Sasi NK, Bhutkar A, Lanning NJ, MacKeigan JP, Weinreich M., Free PMC Article | 02/24/2018 |
| Histone H3 lysine 9 (H3K9) acetylation was most prevalent when the Dbf4 transcription level was highest whereas the H3K9me3 level was greatest during and just after replication. | Dynamic regulation of histone H3K9 is linked to the switch between replication and transcription at the Dbf4 origin-promoter locus.
Kylie K, Romero J, Lindamulage IK, Knockleby J, Lee H., Free PMC Article | 06/24/2017 |
| we propose that phosphorylation of TOP2A by CDC7/DBF4 in early S-phase prevents its localization and/or activity at centromeres, and inhibition of TOP2A function could be relevant to prevent premature separation of centromeric DNA. | DDK dependent regulation of TOP2A at centromeres revealed by a chemical genetics approach.
Wu KZ, Wang GN, Fitzgerald J, Quachthithu H, Rainey MD, Cattaneo A, Bachi A, Santocanale C., Free PMC Article | 06/10/2017 |
| The anti-invasive and cell cycle arrest-inducing effects of nitrogen-containing bisphosphonates are not DBF4 mediated in human breast cancer cells. | The cell cycle arrest and the anti-invasive effects of nitrogen-containing bisphosphonates are not mediated by DBF4 in breast cancer cells.
Mansouri M, Mirzaei SA, Lage H, Mousavi SS, Elahian F. | 10/11/2014 |
| Dbf4 is direct downstream target of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) protein to regulate intra-S-phase checkpoint. | Dbf4 is direct downstream target of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) protein to regulate intra-S-phase checkpoint.
Lee AY, Chiba T, Truong LN, Cheng AN, Do J, Cho MJ, Chen L, Wu X., Free PMC Article | 03/17/2012 |
| bipartite interaction between Cdc7 and Dbf4/ASK subunits facilitates ATP binding and substrate recognition by the Cdc7 kinase. | Molecular mechanism of activation of human Cdc7 kinase: bipartite interaction with Dbf4/activator of S phase kinase (ASK) activation subunit stimulates ATP binding and substrate recognition.
Kitamura R, Fukatsu R, Kakusho N, Cho YS, Taniyama C, Yamazaki S, Toh GT, Yanagi K, Arai N, Chang HJ, Masai H., Free PMC Article | 09/10/2011 |
| Dbf4 regulates the Cdc5 Polo-like kinase through a distinct non-canonical binding interaction | Dbf4 regulates the Cdc5 Polo-like kinase through a distinct non-canonical binding interaction.
Chen YC, Weinreich M., Free PMC Article | 02/26/2011 |
| Data document the role of DBF4 as a key player in nitrogen-containing bisphosphonate-induced cytotoxicity, thus explaining the effects on the cell-cycle. | Identification of secondary targets of N-containing bisphosphonates in mammalian cells via parallel competition analysis of the barcoded yeast deletion collection.
Bivi N, Romanello M, Harrison R, Clarke I, Hoyle DC, Moro L, Ortolani F, Bonetti A, Quadrifoglio F, Tell G, Delneri D., Free PMC Article | 02/22/2010 |
| The interaction with LEDGF relieves autoinhibition of Cdc7-ASK kinase, imposed by the C terminus of ASK. | Transcriptional co-activator LEDGF interacts with Cdc7-activator of S-phase kinase (ASK) and stimulates its enzymatic activity.
Hughes S, Jenkins V, Dar MJ, Engelman A, Cherepanov P., Free PMC Article | 02/1/2010 |
| ASK/Dbf4, a novel cell survival gene in melanoma is transcriptionally regulated by E2F1. | Transcriptional regulation of ASK/Dbf4 in cutaneous melanoma is dependent on E2F1.
Nambiar S, Mirmohammadsadegh A, Hassan M, Hegemann JH, Hengge UR. | 01/21/2010 |
| These results indicate that Ddk functions as an upstream regulator to monitor S-phase checkpoint signaling. | The role of Dbf4/Drf1-dependent kinase Cdc7 in DNA-damage checkpoint control.
Tsuji T, Lau E, Chiang GG, Jiang W., Free PMC Article | 01/21/2010 |
| increased Cdc7-Dbf4 abundance may be a common occurrence in human malignancies | Cdc7-Dbf4 kinase overexpression in multiple cancers and tumor cell lines is correlated with p53 inactivation.
Bonte D, Lindvall C, Liu H, Dykema K, Furge K, Weinreich M., Free PMC Article | 01/21/2010 |
| Cdc7/Dbf4 kinase activity inhibition affects specific phosphorylation sites on MCM2 in cancer cells | Inhibition of Cdc7/Dbf4 kinase activity affects specific phosphorylation sites on MCM2 in cancer cells.
Charych DH, Coyne M, Yabannavar A, Narberes J, Chow S, Wallroth M, Shafer C, Walter AO. | 01/21/2010 |
| A strong origin of replication at the DBF4 promoter locus, which contains two initiation zones, two origin recognition complex (ORC) binding sites and two DNase I-hypersensitive regions, is identified. | Asymmetric bidirectional replication at the human DBF4 origin.
Romero J, Lee H., Free PMC Article | 01/21/2010 |
| There is the differential regulation of a novel gene, namely ASK/Dbf4, in melanoma and suggest that up-regulation of ASK/Dbf4 is a novel molecular determinant with prognostic relevance that confers a proliferative advantage in cutaneous melanoma. | Identification and functional characterization of ASK/Dbf4, a novel cell survival gene in cutaneous melanoma with prognostic relevance.
Nambiar S, Mirmohammadsadegh A, Hassan M, Mota R, Marini A, Alaoui A, Tannapfel A, Hegemann JH, Hengge UR. | 01/21/2010 |
| Results demonstrate a DNA damage checkpoint that targets Cdc7/Dbf4 protein kinase. | An ATR- and Cdc7-dependent DNA damage checkpoint that inhibits initiation of DNA replication.
Costanzo V, Shechter D, Lupardus PJ, Cimprich KA, Gottesman M, Gautier J. | 01/21/2010 |
| results suggest that E2F regulates the ASK promoter through an atypical mode of recognition of the target site | A 63-base pair DNA segment containing an Sp1 site but not a canonical E2F site can confer growth-dependent and E2F-mediated transcriptional stimulation of the human ASK gene encoding the regulatory subunit for human Cdc7-related kinase.
Yamada M, Sato N, Taniyama C, Ohtani K, Arai K, Masai H. | 01/21/2010 |
| Taken together, these results indicate that Cdc7/Dbf4 phosphorylation of MCM2 is essential for the initiation of DNA replication in mammalian cells. | Essential role of phosphorylation of MCM2 by Cdc7/Dbf4 in the initiation of DNA replication in mammalian cells.
Tsuji T, Ficarro SB, Jiang W., Free PMC Article | 01/21/2010 |